1. Absah I. {{The Rates of 61.5% and 38.5% for Vitamin D Deficiency and Insufficiency in Autism, A Guide for Screening in Celiac}}. {Journal of pediatric gastroenterology and nutrition}. 2014 Sep 2.
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2. Ahmed SS, Unland T, Slaven JE, Nitu ME, Rigby MR. {{Successful use of intravenous dexmedetomidine for magnetic resonance imaging sedation in autistic children}}. {Southern medical journal}. 2014 Sep;107(9):559-64.
OBJECTIVES: Autism and autism spectrum disorders (A/ASD) represent a family of neurodevelopmental conditions that are associated with overactive, difficult-to-control behaviors. Sedating these patients for magnetic resonance imaging (MRI) poses challenges. Children with A/ASD were examined against clinical controls to determine the effectiveness and safety of intravenous (IV) dexmedetomidine for deep sedation. METHODS: The quality assurance data on all of the children who received IV dexmedetomidine sedation for MRI between July 2007 and December 2012 were reviewed. Patients in both groups were sedated by an intensivist-based team with a standard plan of 2 mug/kg IV dexmedetomidine administered for 10 minutes followed by an infusion of 1 mug . kg(-1) . hour(-1). The amount of IV dexmedetomidine was titrated to the deep level of sedation. A total of 56 patients in the A/ASD group and 107 in the control group were sedated with no reported sedation failures. Sedation parameters were compared between the A/ASD and control groups using analysis of covariance models, controlling for age, sex, and weight. RESULTS: Children in the A/ASD group were predominantly male (73%) and older (6.1 +/- 0.3 years) than children in the control group (56%; 5.0 +/- 0.2 years; P < 0.05 for both). Procedure time was significantly shorter for patients in the A/ASD group than in control patients (34.6 +/- 2.4 vs 44.3 +/- 1.6 minutes; P < 0.05). The A/ASD and control groups required a similar IV bolus of dexmedetomidine (2.6 mug/kg +/- 0.1 vs 2.4 mug/kg +/- 0.10; P = 0.29), with a significantly lower infusion dose in the A/ASD group (0.74 mug/kg +/- 0.05 vs 0.89 mug/kg +/- 0.03; P < 0.05). Heart rates were similar in the A/ASD group and the control group (67.0 beats per minute +/- 1.6 vs 69.3 +/- 1.1 beats per minute; P = 0.250). There were no complications. Recovery time was approximately 7 minutes longer in the A/ASD group than in the control group, but this was nonsignificant (101.2 +/- 3.5 minutes vs 94.2 +/- 2.4 minutes; P = 0.12). Analyses were performed using analysis of covariance methods and generalized linear models to control for age, sex, and weight. CONCLUSIONS: Children with A/ASD can be successfully sedated for MRIs with IV dexmedetomidine without complications.
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3. Balogh RS, Lake JK, Lin E, Wilton A, Lunsky Y. {{Disparities in diabetes prevalence and preventable hospitalizations in people with intellectual and developmental disability: a population-based study}}. {Diabetic medicine : a journal of the British Diabetic Association}. 2014 Sep 3.
AIMS: To describe and compare population-level aspects of diabetes and diabetes primary care among people with and without intellectual and developmental disabilities. METHODS: Administrative health data accessed from the Institute for Clinical Evaluative Sciences was used to identify a cohort of Ontarians with and without intellectual and developmental disabilities between the ages of 30 and 69 years (n=28 567). These people were compared with a random sample of people without intellectual and developmental disabilities (n=2 261 919) according to diabetes prevalence, incidence, age, sex, rurality, neighbourhood income and morbidity. To measure diabetes primary care, we also studied hospitalizations for diabetes-related ambulatory care-sensitive conditions. RESULTS: Adults with intellectual and developmental disabilities had a consistently higher prevalence and incidence of diabetes than those without intellectual and developmental disabilities. Disparities in prevalence between those with and without intellectual and developmental disabilities were most notable among women, younger adults and those residing in rural or high income neighbourhoods. In terms of hospitalizations for diabetes-related ambulatory care-sensitive conditions, people with intellectual and developmental disabilities were 2.6 times more likely to be hospitalized. CONCLUSIONS: Adults with intellectual and developmental disabilities are at high risk of developing and being hospitalized for diabetes. The findings of the present study have a number of important implications related to the early detection, prevention and proper management of diabetes among adults with intellectual and developmental disabilities. This article is protected by copyright. All rights reserved.
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4. Camacho J, Ejaz E, Ariza J, Noctor SC, Martinez-Cerdeno V. {{RELN-expressing neuron density in layer I of the superior temporal lobe is similar in human brains with autism and in age-matched controls}}. {Neuroscience letters}. 2014 Sep 5;579:163-7.
Reelin protein (RELN) level is reduced in the cerebral cortex and cerebellum of subjects with autism. RELN is synthesized and secreted by a subpopulation of neurons in the developing cerebral cortex termed Cajal-Retzius (CR) cells. These cells are abundant in the marginal zone during cortical development, many die after development is complete, but a small population persists into adulthood. In adult brains, RELN is secreted by the surviving CR cells, by a subset of GABAergic interneurons in layer I, and by pyramidal cells and GABAergic interneurons in deeper cortical layers. It is widely believed that decreased RELN in layer I of the cerebral cortex of subjects with autism may result from a decrease in the density of RELN expressing neurons in layer I; however, this hypothesis has not been tested. We examined RELN expression in layer I of the adult human cortex and found that 70% of cells express RELN in both control and autistic subjects. We quantified the density of neurons in layer I of the superior temporal cortex of subjects with autism and age-matched control subjects. Our data show that there is no change in the density of neurons in layer I of the cortex of subjects with autism, and therefore suggest that reduced RELN expression in the cerebral cortex of subjects with autism is not a consequence of decreased numbers of RELN-expressing neurons in layer I. Instead reduced RELN may result from abnormal RELN processing, or a decrease in the number of other RELN-expressing neuronal cell types.
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5. de Diego-Otero Y, Calvo-Medina R, Quintero-Navarro C, Sanchez-Salido L, Garcia-Guirado F, Del Arco-Herrera I, Fernandez-Carvajal I, Ferrando-Lucas T, Caballero-Andaluz R, Perez-Costillas L. {{A combination of ascorbic acid and alpha-tocopherol to test the effectiveness and safety in the fragile X syndrome: study protocol for a phase II, randomized, placebo-controlled trial}}. {Trials}. 2014 Sep 3;15(1):345.
BACKGROUND: Fragile X syndrome (FXS) is an inherited neurodevelopmental condition characterised by behavioural, learning disabilities, phisical and neurological symptoms. In addition, an important degree of comorbidity with autism is also present. Considered a rare disorder affecting both genders, it first becomes apparent during childhood with displays of language delay and behavioural symptoms.Main aim: To show whether the combination of 10 mg/kg/day of ascorbic acid (vitamin C) and 10 mg/kg/day of alpha-tocopherol (vitamin E) reduces FXS symptoms among male patients ages 6 to 18 years compared to placebo treatment, as measured on the standardized rating scales at baseline, and after 12 and 24 weeks of treatment.Secondary aims: To assess the safety of the treatment. To describe behavioural and cognitive changes revealed by the Developmental Behaviour Checklist Short Form (DBC-P24) and the Wechsler Intelligence Scale for Children-Revised. To describe metabolic changes revealed by blood analysis. To measure treatment impact at home and in an academic environment. METHODS: A phase II randomized, double-blind pilot clinical trial. Scope: male children and adolescents diagnosed with FXS, in accordance with a standardized molecular biology test, who met all the inclusion criteria and none of the exclusion criteria. Instrumentation: clinical data, blood analysis, Wechsler Intelligence Scale for Children-Revised, Conners parent and teacher rating scale scores and the DBC-P24 results will be obtained at the baseline (t0). Follow up examinations will take place at 12 weeks (t1) and 24 weeks (t2) of treatment. DISCUSSION: A limited number of clinical trials have been carried out on children with FXS, but more are necessary as current treatment possibilities are insufficient and often provoke side effects. In the present study, we sought to overcome possible methodological problems by conducting a phase II pilot study in order to calculate the relevant statistical parameters and determine the safety of the proposed treatment. The results will provide evidence to improve hyperactivity control and reduce behavioural and learning problems using ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E). The study protocol was approved by the Regional Government Committee for Clinical Trials in Andalusia and the Spanish agency for drugs and health products.Trial registration: ClinicalTrials.gov Identifier: NCT01329770 (29 March 2011).
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6. Ghanizadeh A. {{The rates of 61.5% and 38.5% for vitamin D deficiency and insufficiency in autism, a guide for screening in celiac}}. {Journal of pediatric gastroenterology and nutrition}. 2014 Sep 2.
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7. Gliga T, Jones EJ, Bedford R, Charman T, Johnson MH. {{From early markers to neuro-developmental mechanisms of autism}}. {Developmental review : DR}. 2014 Sep;34(3):189-207.
A fast growing field, the study of infants at risk because of having an older sibling with autism (i.e. infant sibs) aims to identify the earliest signs of this disorder, which would allow for earlier diagnosis and intervention. More importantly, we argue, these studies offer the opportunity to validate existing neuro-developmental models of autism against experimental evidence. Although autism is mainly seen as a disorder of social interaction and communication, emerging early markers do not exclusively reflect impairments of the « social brain ». Evidence for atypical development of sensory and attentional systems highlight the need to move away from localized deficits to models suggesting brain-wide involvement in autism pathology. We discuss the implications infant sibs findings have for future work into the biology of autism and the development of interventions.
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8. Grein KA, Glidden LM. {{Predicting well-being longitudinally for mothers rearing offspring with intellectual and developmental disabilities}}. {Journal of intellectual disability research : JIDR}. 2014 Sep 3.
BACKGROUND: Well-being outcomes for parents of children with intellectual and developmental disabilities (IDD) may vary from positive to negative at different times and for different measures of well-being. Predicting and explaining this variability has been a major focus of family research for reasons that have both theoretical and applied implications. METHODS: The current study used data from a 23-year longitudinal investigation of adoptive and birth parents of children with IDD to determine which early child, mother and family characteristics would predict the variance in maternal outcomes 20 years after their original measurement. Using hierarchical regression analyses, we tested the predictive power of variables measured when children were 7 years old on outcomes of maternal well-being when children were 26 years old. Outcome variables included maternal self-report measures of depression and well-being. RESULTS: Final models of well-being accounted for 20% to 34% of variance. For most outcomes, Family Accord and/or the personality variable of Neuroticism (emotional stability/instability) were significant predictors, but some variables demonstrated a different pattern. CONCLUSIONS: These findings confirm that (1) characteristics of the child, mother and family during childhood can predict outcomes of maternal well-being 20 years later; and (2) different predictor-outcome relationships can vary substantially, highlighting the importance of using multiple measures to gain a more comprehensive understanding of maternal well-being. These results have implications for refining prognoses for parents and for tailoring service delivery to individual child, parent and family characteristics.
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9. Harrop C. {{Evidence-based, parent-mediated interventions for young children with autism spectrum disorder: The case of restricted and repetitive behaviors}}. {Autism}. 2014 Sep 3.
Restricted and repetitive behaviors represent a core symptom of autism spectrum disorders. While there has been an increase in research into this domain in recent years, compared to social-communication impairments experienced by children with autism spectrum disorders, much less is known about their development, etiology, and management. Parent-mediated interventions have become increasingly popular in the field, with a surge of studies reporting significant findings in social communication and cognitive development in early childhood. Restricted and repetitive behaviors are often not specifically targeted or measured as an outcome within these interventions. This article reviews how 29 parent-mediated interventions approached the management, treatment, and measurement of restricted and repetitive behaviors. Recommendations for research and practice are presented.
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10. Horlin C, Falkmer M, Parsons R, Albrecht MA, Falkmer T. {{The Cost of Autism Spectrum Disorders}}. {PloS one}. 2014;9(9):e106552.
OBJECTIVE: A diagnosis of an autism spectrum disorders is usually associated with substantial lifetime costs to an individual, their family and the community. However, there remains an elusive factor in any cost-benefit analysis of ASD diagnosis, namely the cost of not obtaining a diagnosis. Given the infeasibility of estimating the costs of a population that, by its nature, is inaccessible, the current study compares expenses between families whose children received a formal ASD diagnosis immediately upon suspecting developmental atypicality and seeking advice, with families that experienced a delay between first suspicion and formal diagnosis. DESIGN: A register based questionnaire study covering all families with a child with ASD in Western Australia. PARTICIPANTS: Families with one or more children diagnosed with an ASD, totalling 521 children diagnosed with an ASD; 317 records were able to be included in the final analysis. RESULTS: The median family cost of ASD was estimated to be AUD $34,900 per annum with almost 90% of the sum ($29,200) due to loss of income from employment. For each additional symptom reported, approximately $1,400 cost for the family per annum was added. While there was little direct influence on costs associated with a delay in the diagnosis, the delay was associated with a modest increase in the number of ASD symptoms, indirectly impacting the cost of ASD. CONCLUSIONS: A delay in diagnosis was associated with an indirect increased financial burden to families. Early and appropriate access to early intervention is known to improve a child’s long-term outcomes and reduce lifetime costs to the individual, family and society. Consequently, a per symptom dollar value may assist in allocation of individualised funding amounts for interventions rather than a nominal amount allocated to all children below a certain age, regardless of symptom presentation, as is the case in Western Australia.
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11. Howlin P, Moss P, Savage S, Bolton P, Rutter M. {{Outcomes in Adult Life Among Siblings of Individuals with Autism}}. {J Autism Dev Disord}. 2014 Sep 5.
Little is known about adult siblings of individuals with autism. We report on cognitive, social and mental health outcomes in 87 adult siblings (mean age 39 years). When younger all had been assessed either as being « unaffected » by autism (n = 69) or as meeting criteria for the « Broader Autism Phenotype » (BAP, n = 18). As adults, all scored within the average range on tests of intelligence, numeracy and literacy. « Unaffected » siblings were functioning well in terms of jobs, independence and social relationships. Levels of social relationships and employment were significantly lower in the BAP group; autism traits and mental health problems were significantly higher. The data suggest that the « broader autism phenotype » is a meaningful concept but more sensitive diagnostic measures are required.
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12. Leblond CS, Nava C, Polge A, Gauthier J, Huguet G, Lumbroso S, Giuliano F, Stordeur C, Depienne C, Mouzat K, Pinto D, Howe J, Lemiere N, Durand CM, Guibert J, Ey E, Toro R, Peyre H, Mathieu A, Amsellem F, Rastam M, Gillberg IC, Rappold GA, Holt R, Monaco AP, Maestrini E, Galan P, Heron D, Jacquette A, Afenjar A, Rastetter A, Brice A, Devillard F, Assouline B, Laffargue F, Lespinasse J, Chiesa J, Rivier F, Bonneau D, Regnault B, Zelenika D, Delepine M, Lathrop M, Sanlaville D, Schluth-Bolard C, Edery P, Perrin L, Tabet AC, Schmeisser MJ, Boeckers TM, Coleman M, Sato D, Szatmari P, Scherer SW, Rouleau GA, Betancur C, Leboyer M, Gillberg C, Delorme R, Bourgeron T. {{Meta-analysis of SHANK Mutations in Autism Spectrum Disorders: A Gradient of Severity in Cognitive Impairments}}. {PLoS genetics}. 2014 Sep;10(9):e1004580.
SHANK genes code for scaffold proteins located at the post-synaptic density of glutamatergic synapses. In neurons, SHANK2 and SHANK3 have a positive effect on the induction and maturation of dendritic spines, whereas SHANK1 induces the enlargement of spine heads. Mutations in SHANK genes have been associated with autism spectrum disorders (ASD), but their prevalence and clinical relevance remain to be determined. Here, we performed a new screen and a meta-analysis of SHANK copy-number and coding-sequence variants in ASD. Copy-number variants were analyzed in 5,657 patients and 19,163 controls, coding-sequence variants were ascertained in 760 to 2,147 patients and 492 to 1,090 controls (depending on the gene), and, individuals carrying de novo or truncating SHANK mutations underwent an extensive clinical investigation. Copy-number variants and truncating mutations in SHANK genes were present in approximately 1% of patients with ASD: mutations in SHANK1 were rare (0.04%) and present in males with normal IQ and autism; mutations in SHANK2 were present in 0.17% of patients with ASD and mild intellectual disability; mutations in SHANK3 were present in 0.69% of patients with ASD and up to 2.12% of the cases with moderate to profound intellectual disability. In summary, mutations of the SHANK genes were detected in the whole spectrum of autism with a gradient of severity in cognitive impairment. Given the rare frequency of SHANK1 and SHANK2 deleterious mutations, the clinical relevance of these genes remains to be ascertained. In contrast, the frequency and the penetrance of SHANK3 mutations in individuals with ASD and intellectual disability-more than 1 in 50-warrant its consideration for mutation screening in clinical practice.
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13. Lumeng JC. {{Commentary on « successful use of intravenous dexmedetomidine for magnetic resonance imaging sedation in autistic children »}}. {Southern medical journal}. 2014 Sep;107(9):565-6.
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14. Nevison CD. {{A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors}}. {Environmental health : a global access science source}. 2014 Sep 5;13(1):73.
BACKGROUND: The prevalence of diagnosed autism has increased rapidly over the last several decades among U.S. children. Environmental factors are thought to be driving this increase and a list of the top ten suspected environmental toxins was published recently. METHODS: Temporal trends in autism for birth years 1970-2005 were derived from a combination of data from the California Department of Developmental Services (CDDS) and the United States Individuals with Disabilities Education Act (IDEA). Temporal trends in suspected toxins were derived from data compiled during an extensive literature survey. Toxin and autism trends were compared by visual inspection and computed correlation coefficients. Using IDEA data, autism prevalence vs. birth year trends were calculated independently from snapshots of data from the most recent annual report, and by tracking prevalence at a constant age over many years of reports. The ratio of the snapshot:tracking trend slopes was used to estimate the « real » fraction of the increase in autism. RESULTS: The CDDS and IDEA data sets are qualitatively consistent in suggesting a strong increase in autism prevalence over recent decades. The quantitative comparison of IDEA snapshot and constant-age tracking trend slopes suggests that ~75-80% of the tracked increase in autism since 1988 is due to an actual increase in the disorder rather than to changing diagnostic criteria. Most of the suspected environmental toxins examined have flat or decreasing temporal trends that correlate poorly to the rise in autism. Some, including lead, organochlorine pesticides and vehicular emissions, have strongly decreasing trends. Among the suspected toxins surveyed, polybrominated diphenyl ethers, aluminum adjuvants, and the herbicide glyphosate have increasing trends that correlate positively to the rise in autism. CONCLUSIONS: Diagnosed autism prevalence has risen dramatically in the U.S over the last several decades and continued to trend upward as of birth year 2005. The increase is mainly real and has occurred mostly since the late 1980s. In contrast, children’s exposure to most of the top ten toxic compounds has remained flat or decreased over this same time frame. Environmental factors with increasing temporal trends can help suggest hypotheses for drivers of autism that merit further investigation.
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15. Radeloff D, Ciaramidaro A, Siniatchkin M, Hainz D, Schlitt S, Weber B, Poustka F, Bolte S, Walter H, Freitag CM. {{Structural Alterations of the Social Brain: A Comparison between Schizophrenia and Autism}}. {PloS one}. 2014;9(9):e106539.
Autism spectrum disorder and schizophrenia share a substantial number of etiologic and phenotypic characteristics. Still, no direct comparison of both disorders has been performed to identify differences and commonalities in brain structure. In this voxel based morphometry study, 34 patients with autism spectrum disorder, 21 patients with schizophrenia and 26 typically developed control subjects were included to identify global and regional brain volume alterations. No global gray matter or white matter differences were found between groups. In regional data, patients with autism spectrum disorder compared to typically developed control subjects showed smaller gray matter volume in the amygdala, insula, and anterior medial prefrontal cortex. Compared to patients with schizophrenia, patients with autism spectrum disorder displayed smaller gray matter volume in the left insula. Disorder specific positive correlations were found between mentalizing ability and left amygdala volume in autism spectrum disorder, and hallucinatory behavior and insula volume in schizophrenia. Results suggest the involvement of social brain areas in both disorders. Further studies are needed to replicate these findings and to quantify the amount of distinct and overlapping neural correlates in autism spectrum disorder and schizophrenia.
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16. Reinhardt VP, Wetherby AM, Schatschneider C, Lord C. {{Examination of Sex Differences in a Large Sample of Young Children with Autism Spectrum Disorder and Typical Development}}. {J Autism Dev Disord}. 2014 Sep 5.
Despite consistent and substantive research documenting a large male to female ratio in Autism Spectrum Disorder (ASD), only a modest body of research exists examining sex differences in characteristics. This study examined sex differences in developmental functioning and early social communication in children with ASD as compared to children with typical development. Sex differences in adaptive behavior and autism symptoms were also examined in children with ASD. Participants (n = 511) were recruited from the Florida State University FIRST WORDS(R) Project and University of Michigan Autism and Communication Disorders Center. Analyses did not reveal significant effects of sex or a diagnostic group by sex interaction, suggesting a similar phenotype in males and females early in development. Further research is needed to examine sex differences across development.
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17. Yu TW, Berry-Kravis E. {{Autism and Fragile X Syndrome}}. {Seminars in neurology}. 2014 Jul;34(3):258-65.
Autistic spectrum disorders (ASDs) are characterized by impairments in language, social skills, and repetitive behaviors, often accompanied by intellectual disability. Advances in the genetics of ASDs are providing new glimpses into the underlying neurobiological mechanisms disrupted in these conditions. These glimpses on one hand reinforce the idea that synapse development and plasticity are one of the major pathways disrupted in autism, but beyond that are providing fresh molecular support to the idea of mechanistic parallels between idiopathic ASD and specific syndromic neurodevelopmental disorders like fragile X syndrome (FXS). Fragile X syndrome is already recognized as the most common identifiable genetic cause of intellectual disability and ASDs, with many overlapping phenotypic features. Fragile X syndrome is associated with a variety of cognitive, behavioral, physical, and medical problems, which are managed through supportive treatment. Recent major advances in the understanding of the underlying neurobiology in FXS have led to the discovery of agents that rescue phenotypes in the FXS mouse model, and early clinical trials of targeted treatments in humans with FXS. Thus translational strategies in FXS may be poised to serve as models for ASD and other cognitive disorders.
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18. Zuckerman KE, Sinche B, Cobian M, Cervantes M, Mejia A, Becker T, Nicolaidis C. {{Conceptualization of Autism in the Latino Community and its Relationship with Early Diagnosis}}. {Journal of developmental and behavioral pediatrics : JDBP}. 2014 Sep 1.
OBJECTIVE:: Early identification of autism spectrum disorders (ASD) has been linked to improved long-term developmental outcomes. However, Latino children are diagnosed later than white non-Latino children. We aimed to qualitatively assess the understanding and conceptualization of ASD in the Latino community to understand potential community barriers to early diagnosis. METHODS:: We conducted 5 focus groups and 4 qualitative interviews with 30 parents of typically developing Latino children in Oregon. Participants were asked structured questions concerning video vignettes that follow a Latina mother from the time she begins to worry about her 3-year-old son’s behaviors to the time he receives an ASD diagnosis. Focus groups and interviews were audio-recorded, transcribed, and independently coded. Coded data were analyzed using thematic analysis. RESULTS:: Many Latino families in the study had not heard of ASD or had little information about it. Families sometimes assumed that ASD red flags were normal or could be attributed to family dysfunction. Families also had concerns about provider communication and access to language services. Having a child with a developmental delay was associated with embarrassment, rejection, and family burden, making it difficult for parents to raise developmental concerns with providers. CONCLUSIONS:: Pediatric providers should not assume that Latino parents have heard of ASD or know its symptoms. Providers should be aware that parents may be reluctant to mention concerns because of cultural factors. The health care system needs to improve resources for Latino parents with limited English proficiency. Policies should encourage the use of developmental screening in primary care.
